ArticleMolecular and cellular biology2010
The repressing function of the oncoprotein BCL-3 requires CtBP, while its polyubiquitination and degradation involve the E3 ligase TBLR1.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- NF-κB Signaling in Prostate Cancer Progression: Inflammatory Mediators, Survival Pathways, and Regulatory Axes.Cancers · 2026Review
- Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025Review
- BCL-3 loss sensitises colorectal cancer cells to DNA damage by targeting homologous recombination.DNA repair · 2022Article
- Arsenic trioxide induces proteasome dependent TBLR1-RARα degradation to improve leukemia eradication through cell differentiation enhancement.Journal of Cancer · 2022Article
- Bcl-3: A Double-Edged Sword in Immune Cells and Inflammation.Frontiers in immunology · 2022Review
- The role of B-Cell Lymphoma-3 (BCL-3) in enabling the hallmarks of cancer: implications for the treatment of colorectal carcinogenesis.Carcinogenesis · 2020Review
- BCL-3 promotes a cancer stem cell phenotype by enhancing β-catenin signalling in colorectal tumour cells.Disease models & mechanisms · 2019Article
- Bcl3 Phosphorylation by Akt, Erk2, and IKK Is Required for Its Transcriptional Activity.Molecular cell · 2017Article
- Article
- Cytoplasmic, full length and novel cleaved variant, TBLR1 reduces apoptosis in prostate cancer under androgen deprivation.Oncotarget · 2016Article
- TBL1XR1 in physiological and pathological states.American journal of clinical and experimental urology · 2015Review
- NF-κB-induced KIAA1199 promotes survival through EGFR signalling.Nature communications · 2014Article
- Transducin (β)-like 1 X-linked receptor 1 promotes proliferation and tumorigenicity in human breast cancer via activation of beta-catenin signaling.Breast cancer research : BCR · 2014Article
- MDM2 restrains estrogen-mediated AKT activation by promoting TBK1-dependent HPIP degradation.Cell death and differentiation · 2014Article
- TBLR1 as an androgen receptor (AR) coactivator selectively activates AR target genes to inhibit prostate cancer growth.Endocrine-related cancer · 2014Article
- The tumor promoter and NF-κB modulator Bcl-3 regulates splenic B cell development.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Atypical IκB proteins - nuclear modulators of NF-κB signaling.Cell communication and signaling : CCS · 2013Article
- Expression of Id proteins is regulated by the Bcl-3 proto-oncogene in prostate cancer.Oncogene · 2013Article
- C-Terminal Binding Protein: A Molecular Link between Metabolic Imbalance and Epigenetic Regulation in Breast Cancer.International journal of cell biology · 2013Article
- BCL-3 attenuation of TNFA expression involves an incoherent feed-forward loop regulated by chromatin structure.PloS one · 2013Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear and oncogenic BCL-3 protein activates or represses gene transcription when bound to NF-kappaB proteins p50 and p52, yet the molecules that specifically interact with BCL-3 and drive BCL-3-mediated effects on gene expression remain largely uncharacterized. Moreover, GSK3-mediated phosphorylation of BCL-3 triggers its degradation through the proteasome, but the proteins involved in this degradative pathway are poorly characterized. Biochemical purification of interacting partners of BCL-3 led to the identification of CtBP as a molecule required for the ability of BCL-3 to repress gene transcription. CtBP is also required for the oncogenic potential of BCL-3 and for its ability to inhibit UV-mediated cell apoptosis in keratinocytes. We also defined the E3 ligase TBLR1 as a protein involved in BCL-3 degradation through a GSK3-independent pathway. Thus, our data demonstrate that the LSD1/CtBP complex is required for the repressing abilities of an oncogenic I kappaB protein, and they establish a functional link between the E3 ligase TBLR1 and NF-kappaB.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.